11633 RESULTS
COMMENT Elena Cattaneo’s beautiful paper in Science (Zuccato et al., 2001) demonstrated clearly that in transfected cells and in transgenic animals, wild-type and mutant huntingtin modulate BDNF transcription in opposite directions. In conditionally immortalized
COMMENT Cortico-Cortical Connectivity: A Key Aspect to Neurodegeneration The work from William Yang and colleagues (Gu et al., 2005), while directed toward Huntington’s disease (HD), is likely broadly applicable to a number of neurodegenerative disorders includin
COMMENT Rosch and colleagues in the May 17 issue of PNAS provide intriguing new data implicating p75NTR in activity-dependent synaptic plasticity. The authors use two strains of p75NTR mutants (p75NTRexonIV-/- and p75NTRexonII-/-) to investigate the emerging conc
COMMENT The Wheel of Death: Neuronal Cell Cycle and Alzheimer Disease There are multiple unanswered questions related to the pathogenesis of Alzheimer disease (AD). However, a major step forward in answering at least three important aspects was recently provided
COMMENT The observation that DJ-1 is capable of protecting cells against oxidant-induced cell death has been confirmed in several laboratories without a very clear mechanism emerging for how this would happen. Showing that simple scavenging of radicals is not lik
COMMENT This mouse model seems to be a powerful tool to study different issues, the relationship between AD and lipids included. I am only surprised that cholesterol keeps being labelled as a risk factor for AD, despite the fact that in light of numerous old and
COMMENT This report by Vivian Budnik and coworkers provides some new insight into the normal roles of FasII, APPL and X11 in synapse formation, but it is especially interesting for AD researchers because of its potential insight into the mechanism of dystrophic n
COMMENT paper, the authors of the commented study at the first place, but also Drs. Koudinov and Koudinova, who
COMMENT I have a scientific question: How can aging be a risk factor for Alzheimer's? Diseases have causes, don't they? 1. Most aging humans don't get AD, and no wild animals, eating natural foods, get it, whatever their age. That includes chimps.
COMMENT The work described in this abstract appears to make a nice dissection of age vs. strain effects in gene expression profiles and mutations. 0 Paul_Coleman
COMMENT This is a very good paper offering further support for the role of infection-induced inflammation in triggering neurological impairment at the level of memory consolidation in the hippocampus. Interestingly, the authors obtained results indicating that th
COMMENT McMahon et al. present convincing evidence of a connection between a neurodegenerative, trinucleotide expansion repeat disorder, spinocerebellar ataxia 7, and chromatin-dependent gene activation. Sgf73 is a key component of the SAGA and SLIK transcription
COMMENT This is a most interesting and provocative study. It adds yet another wrinkle to the AD pathology cascade and suggests that cell cycle re-expression may be a major factor in the eventual cell death seen in AD. Data generated from our laboratory showing ne
COMMENT I am an AD patient, age 29. All decision-making should include me. I am documenting now how future illness should or should not be treated when I am incapable of making those decisions. 0 cookywomyn
COMMENT If a disturbed cell cycle was a primary "cause" of AD, as Webber et al. conjecture, how could this explain the phenomenon of twin discordance, or different AD rates in different populations? If Webber et al. cannot take into account such factors
